Taste-aversion learning has been a popular paradigm for examining associative processes because it often produces outcomes that are different from those observed in other classical conditioning paradigms. One such outcome is taste-mediated odor potentiation in which aversion conditioning with a weak odor and a strong taste results in increased or synergistic conditioning to the odor. Because this strengthened odor aversion was not anticipated by formal models of learning, investigation of taste-mediated odor potentiation was a hot topic in the (...) 1980s. The present manuscript reviews the history of potentiation research with particular focus given to the stimuli that produce potentiation, the conditions that produce potentiation, the possible mechanism of this phenomenon, and possible reasons for the decline of research in this area. Although the number of published reports of potentiation has decreased since the 1980s, recent physiological and behavioral assessments have advanced the field considerably, and the opportunities for future research are bountiful. Recent physiological experiments, for example, have identified the basolateral nucleus of the amygdala as the key brain region to produce taste-mediated odor potentiation (e.g., Hatfield andGallagher, 1995). Also, recent behavioral experiments have extended the generality of synergistic conditioning effects. Studies have shown that odor can potentiate responding to taste (Slotnick, Westbrook and Darling, 1997) and that augmented responding can be produced in the A+/AX+blocking design (e.g., Batsell and Batson, 1999). With the current understanding of where synergistic conditioning may occur in the brain and the new tools to explore synergistic conditioning, we propose various directions for future research to determine whether taste-aversion learning and synergistic conditioning require unique explanations. (shrink)

Taste-aversion learning has been a popular paradigm for examining associative processes because it often produces outcomes that are different from those observed in other classical conditioning paradigms. One such outcome is taste-mediated odor potentiation in which aversion conditioning with a weak odor and a strong taste results in increased or synergistic conditioning to the odor. Because this strengthened odor aversion was not anticipated by formal models of learning, investigation of taste-mediated odor potentiation was a hot topic in the (...) 1980s. The present manuscript reviews the history of potentiation research with particular focus given to the stimuli that produce potentiation, the conditions that produce potentiation, the possible mechanism of this phenomenon, and possible reasons for the decline of research in this area. Although the number of published reports of potentiation has decreased since the 1980s, recent physiological and behavioral assessments have advanced the field considerably, and the opportunities for future research are bountiful. Recent physiological experiments, for example, have identified the basolateral nucleus of the amygdala as the key brain region to produce taste-mediated odor potentiation (e.g., Hatfield andGallagher, 1995). Also, recent behavioral experiments have extended the generality of synergistic conditioning effects. Studies have shown that odor can potentiate responding to taste (Slotnick, Westbrook and Darling, 1997) and that augmented responding can be produced in the A+/AX+blocking design (e.g., Batsell and Batson, 1999). With the current understanding of where synergistic conditioning may occur in the brain and the new tools to explore synergistic conditioning, we propose various directions for future research to determine whether taste-aversion learning and synergistic conditioning require unique explanations. (shrink)

Taste-aversion learning has been a popular paradigm for examining associative processes because it often produces outcomes that are different from those observed in other classical conditioning paradigms. One such outcome is taste-mediated odor potentiation in which aversion conditioning with a weak odor and a strong taste results in increased or synergistic conditioning to the odor. Because this strengthened odor aversion was not anticipated by formal models of learning, investigation of taste-mediated odor potentiation was a hot topic in the (...) 1980s. The present manuscript reviews the history of potentiation research with particular focus given to the stimuli that produce potentiation, the conditions that produce potentiation, the possible mechanism of this phenomenon, and possible reasons for the decline of research in this area. Although the number of published reports of potentiation has decreased since the 1980s, recent physiological and behavioral assessments have advanced the field considerably, and the opportunities for future research are bountiful. Recent physiological experiments, for example, have identified the basolateral nucleus of the amygdala as the key brain region to produce taste-mediated odor potentiation. Also, recent behavioral experiments have extended the generality of synergistic conditioning effects. Studies have shown that odor can potentiate responding to taste and that augmented responding can be produced in the A+ /AX+blocking design. With the current understanding of where synergistic conditioning may occur in the brain and the new tools to explore synergistic conditioning, we propose various directions for future research to determine whether taste-aversion learning and synergistic conditioning require unique explanations. (shrink)

The cellular basis of motor learning in the cerebellum has been attributed mostly to long-term depression (LTD) at excitatory parallel fiber (PF)-Purkinje cell (PC) synapses. LTD is induced when PFs are activated in conjunction with a climbing fiber (CF), the other excitatory input to PCs. Recently, by using whole-cell patch-clamp recording from PCs in cerebellar slices, a new form of synaptic plasticity was discovered. Stimulation of excitatory CFs induced a long-lasting (usually longer than 30 min) of 30 sec) and the (...) durations of RP (>30 min) strongly suggests that some intracellular biochemical machinery is involved. Pharmacological evidence suggests that protein kinases are involved in RP of inhibitory synapses and LTD of excitatory PF synapses. Besides the well-described LTD, RP could be a cellular mechanism that plays an important role in motor learning. (shrink)

The structuralist program has developed a useful metascientific resource: ontological reductive links (ORLs) between the constituents of the potential models of reduced and reducing theories. This resource was developed initially to overcome an objection to structuralist ``global'' accounts of the intertheoretic reduction relation. But it also illuminates the way that concepts at a higher level of scientific investigation (e.g., cognitive psychology) become ``structured through reduction'' to lower-level investigations (e.g., cellular/molecular neuroscience). After (briefly) explaining this structuralist background, I demonstrate how this (...) resource illuminates an actual, emerging scientific example: the link between the psychological concept of a ``consolidation switch'' from short-term to long-term memory and the cellular/molecular mechanisms of the transition from early- to late-phases of long-term potentiation (LTP) (an important type of synaptic plasticity in mammalian hippocampus and cortex). (shrink)

Long-term potentiation (LTP) is operationally defined as a long-lasting increase in synaptic efficacy following high-frequency stimulation of afferent fibers. Since the first full description of the phenomenon in 1973, exploration of the mechanisms underlying LTP induction has been one of the most active areas of research in neuroscience. Of principal interest to those who study LTP, particularly in the mammalian hippocampus, is its presumed role in the establishment of stable memories, a role consistent with descriptions of memory formation. Other (...) characteristics of LTP, including its rapid induction, persistence, and correlation with natural brain rhythms, provide circumstantial support for this connection to memory storage. Nonetheless, there is little empirical evidence that directly links LTP to the storage of memories. In this target article we review a range of cellular and behavioral characteristics of LTP and evaluate whether they are consistent with the purported role of hippocampal LTP in memory formation. We suggest that much of the present focus on LTP reflects a preconception that LTP is a learning mechanism, although the empirical evidence often suggests that LTP is unsuitable for such a role. As an alternative to serving as a memory storage device, we propose that LTP may serve as a neural equivalent to an arousal or attention device in the brain. Accordingly, LTP may increase in a nonspecific way the effective salience of discrete external stimuli and may thereby facilitate the induction of memories at distant synapses. Other hypotheses regarding the functional utility of this intensely studied mechanism are conceivable; the intent of this target article is not to promote a single hypothesis but rather to stimulate discussion about the neural mechanisms underlying memory storage and to appraise whether LTP can be considered a viable candidate for such a mechanism. (shrink)

The type I CaM-sensitive adenylyl cyclase is in a position to integrate signals from multiple inputs, consistent with the requirements for mediating long term potentiation (LTP). Biochemical and genetic evidence supports the idea that this enzyme plays an important role inc LTP. However, more work is needed before we will be certain of the role that CaM-sensitive adenylyl cyclases play in LTP.

Shors & Matzel's target article is a thought-provoking attempt to reconceptualise long-term potentiation as an attentional or arousal mechanism rather than a memory storage mechanism. This is incompatible with the facts of the neurobiology of attention and of the behavioural neurophysiological properties of hippocampal neurons.

In the thirty years since its discovery by Terje Lomo and Tim Bliss, Long Term Potentiation has become one of the most extensively studied topics in contemporary neuroscience. In LTP the strength of synapses between neurons is potentiated following brief but intense activation. LTP is thought to play a central role in learning and memory, though the exact nature of its role is less clear. In spite of years of research, there are many questions about LTP regarding its functional (...) relevance that remain unanswered - for example, is it a model of memory formation, or is the actual neural mechanism used by the brain to store information? This volume presents a state of the art account of LTP. It begins with lively accounts, by the scientists most closely involved, of the discovery of LTP and of the experiments that established its basic properties and induction mechanisms. Later contributions contain reviews and new research that cover the range of molecular, cellular, physiological and behavioural approaches to the study of LTP. Provocative, accessible, and authoritative, this book makes it clear why LTP continues in equal measure to puzzle and beguile neuroscientists today. Advance praise for Long Term Potentiation: 'This book provides a definitive overview of the development of ideas about synaptic plasticity and about the wide range of current research in this fascinating field.' Colin Blakemore, University of OxfordReadership: Neuroscientists from postgraduate level upwards. (shrink)

The phenomenon of synesthesia has undergone an invigoration of research interest and empirical progress over the past decade. Studies investigating the cognitive mechanisms underlying synesthesia have yielded insight into neural processes behind such cognitive operations as attention, memory, spatial phenomenology and inter-modal processes. However, the structural and functional mechanisms underlying synesthesia still remain contentious and hypothetical. The first section of the present paper reviews recent research on grapheme-color synesthesia, one of the most common forms of synesthesia, and addresses the ongoing (...) debate concerning the role of selective attention in eliciting synesthetic experience. Drawing on conclusions of the first half, the paper’s second half examines the various models proposed to explain the cognitive mechanisms behind grapheme-color synesthesia, and discusses the explanatory virtues of a new model suggesting that grapheme-color synesthesia is grounded in memory. The last section offers an examination of some of the broader philosophical implications of synesthesia. (shrink)

Shors & Matzel set up a straw man, that LTP is a memory storage mechanism, and knock him down without due consideration of the important relations among different levels of organization and analysis regarding LTP, learning, and memory. Assessing these relationships requires analysis and hypotheses linking specific brain regions, neural circuits, plasticity mechanisms, and task demands. The issue addressed by the authors is important, but their analysis is off target.

Shors & Matzel propose that hippocampal LTP increases the effective salience of discrete external stimuli and thereby facilitates the induction of memories at distant places. In line with this suggestion, a neural network model of associative learning and hippocampal function assumes that LTP increases hippocampal error signals to the cortex, thereby facilitating stimulus configuration in association cortex. Computer simulations show that under these assumptions the model correctly describes the effect of LTP induction and blockade in classical discriminations and place learning.

Pains that persist long after damaged tissue hasrecovered remain a perplexing phenomenon. Theseso-called chronic pains serve no useful function foran organism and, given its disabling effects, mighteven be considered maladaptive. However, a remarkablesimilarity exists between the neural bases thatunderlie the hallmark symptoms of chronic pain andthose that subserve learning and memory. Bothphenomena, wind-up in the pain literature andlong-term potentiation (LTP) in the learning andmemory literature, are forms of neuroplasticity inwhich increased neural activity leads to a longlasting increase in the (...) excitability of neuronsthrough structural modifications at pre- andpost-synaptic sites. Moreover, the synapticmodifications of wind-up and LTP share a commonmechanism: a glutamate N -methyl-D-aspartate(NMDA) receptor interaction that initiates a calciummediated biochemical cascade that ultimately enhancessignal processing at the -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) receptor. This paper arguesthat chronic pain, which has no adaptive value, canbe accounted for in terms of the highly adaptivephenomenon of activity-dependent neural plasticity;hence, some cases of chronic pain can beconceptualized as a memory trace in spinal neurons. (shrink)

Evidence from invertebrate systems including Aplysia and Drosophila, as well as studies carried out with mammalian brain, suggests that Ca2+-sensitive adenylyl cyclases may be important for long-term synaptic changes and learning and memory. Furthermore, some forms of long-term potentiation (LTP) in the hippocampus elevate cyclic AMP (cAMP) signals, and activation of adenylyl cyclases and cAMP-dependent protein kinase may be required for late stages of LTP. We propose that long-term changes in neurons and at synapses may require synergism between the (...) cAMP and Ca2+ signal transduction systems which regulates transcription and synthesis of specific proteins required for long-term synaptic changes. During LTP, protein kinase C is activated and intraccllular Ca2+ increases. We hypothesize that the calmodulin (CaM)-regulated adenylyl cyclases may be activated during LTP because of increases in intracellular Ca2+, release of free CaM from neuromodulin, activation by protein kinase C, release of neurotransmitters, or a combination of these events. Synergistic activation of CaM-sensitive adenylyl cyclases may produce a robust or prolonged cAMP signal required for transcriptional control. Furthermore, the coupling of the Ca2+ and cAMP systems may provide positive feedback regulation of Ca2+ channels by cAMP-dependent protein kinase. (shrink)

As opposed to the dismissive attitude toward reductionism that is popular in current philosophy of mind, a “ruthless reductionism” is alive and thriving in “molecular and cellular cognition”—a field of research within cellular and molecular neuroscience, the current mainstream of the discipline. Basic experimental practices and emerging results from this field imply that two common assertions by philosophers and cognitive scientists are false: (1) that we do not know much about how the brain works, and (2) that lower-level neuroscience cannot (...) explain cognition and complex behavior directly. These experimental practices involve intervening directly with molecular components of sub-cellular and gene expression pathways in neurons and then measuring specific behaviors. These behaviors are tracked using tests that are widely accepted by experimental psychologists to study the psychological phenomenon at issue (e.g., memory, attention, and perception). Here I illustrate these practices and their importance for explanation and reduction in current mainstream neuroscience by describing recent work on social recognition memory in mammals. (shrink)

It has been 35 years since the publicationMelzack and Wall's Gate Control Theory whichhypothesized that nociceptive information wassubject to dynamic regulation by mechanismslocated in the spinal cord dorsal horn thatcould ultimately lead to hyperalgesic orhypoalgesic states. This paper examines GateControl Theory in light of our currentunderstanding of the neuroanatomical,neurophysiological and neurochemical substratesof nociception and antinociception. Despiteits initial controversies, no one has proposeda more comprehensive overall theory of painmodulation or has successfully refuted most ofthe basic tenets of this theory.

It is argued that John Bickle’s Ruthless Reductionism is flawed as an account of the practice of neuroscience. Examples from genetics and linguistics suggest, first, that not every mind-brain link or gene-phenotype link qualifies as a reduction or as a complete explanation, and, second, that the higher (psychological) level of analysis is not likely to disappear as neuroscience progresses. The most plausible picture of the evolving sciences of the mind-brain seems a patchwork of multiple connections and partial explanations, linking anatomy, (...) mechanisms and functions across different domains, levels, and grain sizes. Bickle’s claim that only the molecular level provides genuine explanations, and higher level concepts are just heuristics that will soon be redundant, is thus rejected. In addition, it is argued that Bickle’s recasting of philosophy of science as metascience explicating empirical practices, ignores an essential role for philosophy in reflecting upon criteria for reduction and explanation. Many interesting and complex issues remain to be investigated for the philosophy of science, and in particular the nature of interlevel links found in empirical research requires sophisticated philosophical analysis. (shrink)

Philosophers of neuroscience have traditionally described interfield integration using reduction models. Such models describe formal inferential relations between theories at different levels. I argue against reduction and for a mechanistic model of interfield integration. According to the mechanistic model, different fields integrate their research by adding constraints on a multilevel description of a mechanism. Mechanistic integration may occur at a given level or in the effort to build a theory that oscillates among several levels. I develop this alternative model using (...) a putative exemplar of reduction in contemporary neuroscience: the relationship between the psychological phenomena of learning and memory and the electrophysiological phenomenon known as Long-Term Potentiation. A new look at this historical episode reveals the relative virtues of the mechanistic model over reduction as an account of interfield integration. (shrink)

Research in the neurosciences continues to provide evidence that sleep plays a role in the processes of learning and memory. There is less of a consensus, however, regarding the precise stages of memory development during which sleep is considered a requirement, simply favorable, or not important. This article begins with an overview of recent studies regarding sleep and learning, predominantly in the procedural memory domain, and is measured against our current understanding of the mechanisms that govern memory formation. Based on (...) these considerations, I offer a new neurocognitive framework of procedural learning, consisting first of acquisition, followed by two specific stages of consolidation, one involving a process of stabilization, the other involving enhancement, whereby delayed learning occurs. Psychophysiological evidence indicates that initial acquisition does not rely fundamentally on sleep. This also appears to be true for the stabilization phase of consolidation, with durable representations, resistant to interference, clearly developing in a successful manner during time awake (or just time, per se). In contrast, the consolidation stage, resulting in additional/enhanced learning in the absence of further rehearsal, does appear to rely on the process of sleep, with evidence for specific sleep-stage dependencies across the procedural domain. Evaluations at a molecular, cellular, and systems level currently offer several sleep specific candidates that could play a role in sleep-dependent learning. These include the upregulation of select plasticity-associated genes, increased protein synthesis, changes in neurotransmitter concentration, and specific electrical events in neuronal networks that modulate synaptic potentiation. Key Words: consolidation; enhancement; learning; memory; plasticity; sleep; stabilization. (shrink)

Because little is known about the human trait of affiliation, we provide a novel neurobehavioral model of affiliative bonding. Discussion is organized around processes of reward and memory formation that occur during approach and consummatory phases of affiliation. Appetitive and consummatory reward processes are mediated independently by the activity of the ventral tegmental area (VTA) dopamine (DA)–nucleus accumbens shell (NAS) pathway and the central corticolimbic projections of the u-opiate system of the medial basal arcuate nucleus, respectively, although these two projection (...) systems functionally interact across time. We next explicate the manner in which DA and glutamate interact in both the VTA and NAS to form incentive-encoded contextual memory ensembles that are predictive of reward derived from affiliative objects. Affiliative stimuli, in particular, are incorporated within contextual ensembles predictive of affiliative reward via: (a) the binding of affiliative stimuli in the rostral circuit of the medial extended amygdala and subsequent transmission to the NAS shell; (b) affiliative stimulus-induced opiate potentiation of DA processes in the VTA and NAS; and (c) permissive or facilitatory effects of gonadal steroids, oxytocin (in interaction with DA), and vasopressin on (i) sensory, perceptual, and attentional processing of affiliative stimuli and (ii) formation of social memories. Among these various processes, we propose that the capacity to experience affiliative reward via opiate functioning has a disproportionate weight in determining individual differences in affiliation. We delineate sources of these individual differences, and provide the first human data that support an association between opiate functioning and variation in trait affiliation. Key Words: affiliation corticolimbic-striatal networks; appetitive and consummatory reward; dopamine; oxytocin; personality; social bonds; social memory; u-opiates. (shrink)

Long-Term Potentiation (LTP) is a kind of synaptic plasticity that many contemporary neuroscientists believe is a component in mechanisms of memory. This essay describes the discovery of LTP and the development of the LTP research program. The story begins in the 1950's with the discovery of synaptic plasticity in the hippocampus (a medial temporal lobe structure now associated with memory), and it ends in 1973 with the publication of three papers sketching the future course of the LTP research program. (...) The making of LTP was a protracted affair. Hippocampal synaptic plasticity was initially encountered as an experimental tool, then reported as a curiosity, and finally included in the ontic store of the neurosciences. Early researchers were not investigating the hippocampus in search of a memory mechanism; rather, they saw the hippocampus as a useful experimental model or as a structure implicated in the etiology of epilepsy. The link between hippocampal synaptic plasticity and learning or memory was a separate conceptual achievement. That link was formulated in at least three different ways at different times: reductively (claiming that plasticity is identical to learning), analogically (claiming that plasticity is an example or model of learning), and mechanistically (claiming that plasticity is a component in learning or memory mechanisms). The hypothesized link with learning or memory, coupled with developments in experimental techniques and preparations, shaped how researchers understood LTP itself. By 1973, the mechanistic formulation of the link between LTP and memory provided an abstract framework around which findings from multiple perspectives could be integrated into a multifield research program. (shrink)

We argue in this paper that so-called new wave reductionism fails to capture the nature of the interlevel relations between psychology and neuroscience. Bickle (1995, Psychoneural reduction of the genuinely cognitive: some accomplished facts, Philosophical Psychology, 8, 265-285; 1998, Psychoneural reduction: the new wave, Cambridge, MA: MIT Press) has claimed that a (bottom-up) reduction of the psychological concepts of learning and memory to the concepts of neuroscience has in fact already been accomplished. An investigation of current research on the phenomenon (...) of long-term potentiation reveals that this claim overstates the facts. Both the psychological and the neural concepts involved have not yet stabilized and face further correction under the influence of both bottom-up and top-down selection pressures. In addition, psychological concepts often refer to functions, and functions are indispensable and irreducible. Function ascriptions pick out objective patterns involving historical factors and distal goals. This view of functions implies that psychological facts cannot be simply read off from the neurophysiological facts. Although psychological theorizing is constrained by neurophysiology (and vice versa), psychology remains distinct at least to some degree. (shrink)

The scientific method is a potentiation of common sense, exercised with a specially firm determination not to persist in error if any exertion of hand or mind can deliver us from it. We are all affected by our past. I grew up in the “Land of Lincoln,” so stories about the 16th U.S. President, “Honest Abe” as we called him, were unavoidable in my youth. In particular, we learned that Abraham Lincoln never told a lie. Well, one day when (...) I was 10, a friend caused a bike accident that broke my left clavicle. When my parents asked me what had happened, I lied. I told them that I fell against the corner of a building. As I recall, I lied in order to protect my friend. His family was very poor, and my young mind .. (shrink)

Insights into the role of sleep in the molecular mechanisms of memory consolidation may come from studies of activity-dependent synaptic plasticity, such as long-term potentiation (LTP). This commentary posits a specific contribution of sleep to LTP stabilization, in which mRNA transported to dendrites during wakefulness is translated during sleep. Brain-derived neurotrophic factor may drive the translation of newly transported and resident mRNA.

It has been suggested that type I adenylyl cyclase may play a unique role in long-term potentiation, due to both unique regulatory properties as well as a specialized distribution within the mammalian brain. This would allow an integration of the signals wrought by increased intracellular calcium with those conveyed into the cellular milieu via increased cAMP. These results are discussed in the context of changes in cellular structure, because of changing interactions between G proteins and cytoskeletal components, which might (...) be expected to accompany chronic synaptic activation. (shrink)

We propose that sleep is linked to synaptic homeostasis. Specifically, we propose that: (1) Wakefulness is associated with synaptic potentiation in cortical circuits; (2) synaptic potentiation is tied to the homeostatic regulation of slow wave activity; (3) slow wave activity is associated with synaptic downscaling; and (4) synaptic downscaling is tied to several beneficial effects of sleep, including performance enhancement.

Our results on hippocampal long-term potentiation are considered in the context of Xia et al.'s hypothesis. Whereas the target article proposes presynaptic PKC involvement in adenylyl cyclase activation by phosphorylation of nenromodulin, we suggest an additional postsynaptic role involving RC3/nenrogranin. Finally, we examine the possibility that the adenylyl cyclase mutant mouse may display normal learning with a selective impairment of memory.

The regulatory properties of the neurospecific, type I adenylyl cyclase and its distribution within brain have suggested that this enzyme may be important for neuroplasticity. To address this issue, the murine, Ca2+ -stimulated adenylyl cyclase (type I), was inactivated by targeted mutagenesis. Ca2+ -stimulated adenylyl cyclase activity was reduced 40% to 60% in the hippocampus, neocortex, and cerebellum. Long term potentiation in the CA1 region of the hippocampus from mutants was perturbed relative to controls. Both the initial slope and (...) maxim um extent of changes in synaptic response were reduced. Although mutant mice learned to find a hidden platform normally in the Morris water task, they did not display a preference for the region where the platform had been when it was removed. The behavioral phenotype of these mice is very similar to that exhibited by mice which have been surgically lesioned in the hippocampus. These results indicate that disruption of the gene for the type I adenylyl cyclase produces changes in spatial memory and indicate that the cAMP signal transduction pathway may play an important role for synaptic plasticity. (shrink)

Evidence is summarised for and against the hypothesis that potentiation or facilitation of neural responses during a train of threshold-level stimuli occurred in the experiments reported by Libet et al. . It is concluded that such potentiation probably did occur. Since the main arguments for the existence of subjective backwards referral take it as given that such potentiation did not occur, it is further concluded that the main arguments for the existence of subjective backwards referral fail.

The neurophysiological phenomenon of LTP (long term potentiation) is considered by many to represent an adequate mechanism for acquiring or storing memories in the mammalian brain. In our target article, we reviewed the various arguments put forth in support of the LTP/memory hypothesis. We concluded that these arguments were inconsistent with the purported data base and proposed an alternative interpretation that we suggested was at least as compatible with the available data as the more widely held view. In doing (...) so, we attempted to illustrate that the inadequacy of present experimental designs did not permit us to distinguish between equally viable hypotheses. In the four years since we wrote the first draft of our target article, hundreds of additional studies on LTP have been published and their results have been incorporated into current theories about memory. A diverse group of commentators responded to our target article with their own theories of how memories might be stored in the brain, some of which rely on LTP. Some commentators doubted whether memories can be stored through modifications of synaptic strength. Some assert that it will never be possible to understand the neural mechanisms of memory; still others remain hopeful that we will accomplish some semblance of a resolution, provided we appreciate LTP's role in a subset of seemingly amorphous memory systems. In summary, although it is commonly written that “LTP is a memory storage device,” the divergence of views among the commentators suggests, at least as strongly as our target article, that such conviction is unwarranted and fails to acknowledge both the lack of consensus regarding the role of LTP in memory and the complexity of the phenomenon of memory itself. (shrink)

Shors & Matzel provide compelling arguments against a role for hippocampal long-term potentiation (LTP) in mammalian learning and memory. As an alternative, they suggest that LTP is an arousal mechanism. I will argue that this view is not a satisfactory alternative to current conceptions of LTP function.

Many philosophers and neuroscientists defend a view we express with the slogan that mental science is neuroscience. We argue that there are two ways of interpreting this view, depending on what is meant by ‘neuroscience’. On one interpretation, the view is that mental science is cognitive neuroscience, where this is the science that integrates psychology with the biology of the brain. On another interpretation, the view is that mental science is biological neuroscience, where this is the investigation concerned with the (...) chemistry, physiology and anatomy of neurons and neuronal assemblies. Since the claim about cognitive neuroscience is a scientific triviality, we concentrate on the claim about biological neuroscience, and criticise two initially promising lines of argument for it, one prompted by reflection on the history of biology, and one prompted by reflection on the neurophysiological process known as long‐term potentiation, which may be implicated in learning. We argue that neither of these arguments is successful in supporting the view that mental science is biological neuroscience. (shrink)

Long-term potentiation (LTP) is a long-lasting increase in synaptic efficacy that many consider the best candidate currently available for a neural mechanism of memory formation and/or storage in the mammalian brain. In our target article, LTP: What's learning got to do with it?, we concluded that there was insufficient data to warrant such a conclusion. In their commentaries, Jeffery and Zhadin raise a number of important issues that we did not raise, both for and against the hypothesis. Although we (...) agree with a number of these issues, we maintain that there remains insufficient evidence that LTP is a memory mechanism. (shrink)

There is no general agreement as to the meaning of long-term potentiation, but this cannot be resolved by using it to explain additional phenomena. Increased attention to recently experienced stimuli is a form of learning known to neuropsychologists as repetition priming. As more is learned about the neurochemistry of synaptic change, the term LTP will wither.